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<v Speaker 1>Today we're gonna be going over gastric disorders, so it's

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<v Speaker 1>going to be involving gastritis, peptic ulcer disease, and pyloric stenosis.

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<v Speaker 1>And I just want to mention really quick, if you

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<v Speaker 1>do like the podcast, it's helping you. Please, please, if

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<v Speaker 1>you wouldn't mind giving me a review on Apple Podcasts, Spotify,

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<v Speaker 1>just let me know that it's helping you. It kind

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<v Speaker 1>of also gets the word out about the podcast and

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<v Speaker 1>helps other people discovered as well. I'd really appreciate that.

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<v Speaker 1>So with that being said, let's go ahead and start

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<v Speaker 1>with aqte gastritis. So qute gastritis is an inflammation resulting

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<v Speaker 1>from gastric mucosal injury. It's important to note that there

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<v Speaker 1>is something else called gastropathy, which is going to be

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<v Speaker 1>a more superficial mucosal injury with no associated inflammation. So

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<v Speaker 1>that's another term that you need to know as well.

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<v Speaker 1>As far as eteologies, H pylori most common cause by

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<v Speaker 1>far H pylori. Remember this is going to be your

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<v Speaker 1>most common cause of acte gastritis.

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<v Speaker 2>And H.

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<v Speaker 1>Pylori is a GRAM negative bacteria that's very common. It's

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<v Speaker 1>actually found in about half of the world's population, So

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<v Speaker 1>not everybody gets symptoms from this though, So just because

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<v Speaker 1>it's part of your microbio doesn't mean you're gonna have symptoms,

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<v Speaker 1>but the people that do develop symptoms. H Pylori infects

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<v Speaker 1>the gastric mucosa. It releases certain enzymes and toxins, and

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<v Speaker 1>it injures the epithelial cells of the stomach, which leaves

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<v Speaker 1>the stomach more vulnerable to the acid that's present and

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<v Speaker 1>causes gastritis. It can cause peptic ulcers as well as

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<v Speaker 1>pain and a number of other symptoms. So that's how

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<v Speaker 1>H bilori causes that. Again, most common cause. That keep

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<v Speaker 1>repeating it because it's important. And then your second most

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<v Speaker 1>common cause is going to be from n seds and aspirin.

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<v Speaker 1>So the way n seds and aspirin and cause gastritis

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<v Speaker 1>one way is that it's just from a superficial irritation

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<v Speaker 1>of the epithelium of the gastric mucosa. So that can

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<v Speaker 1>happen if you take like eight hundred milligrams vibuprof and

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<v Speaker 1>you didn't any food with it, and you just have

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<v Speaker 1>this stomach pain for a couple hours. But the more

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<v Speaker 1>important factor is that n sets inhibit COX one production,

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<v Speaker 1>so COX one production is actually responsible for producing prostag landins.

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<v Speaker 1>So if you decrease COX one production, decrease production of

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<v Speaker 1>prostic landings. Well, why does that matter. It's because prostac

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<v Speaker 1>landins actually inhibit gastric acid secretion, so less prostac landins

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<v Speaker 1>means more gastric acid and more irritation like gastritis peptic ulcers.

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<v Speaker 1>So that's why n sets are really important as a

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<v Speaker 1>factor that can cause gastritis. And that's actually why n

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<v Speaker 1>sets like celebres, which is also known as celocoxid, were

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<v Speaker 1>created because celebres actually targets COX two rather than COX one,

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<v Speaker 1>So this leads to less gastric issues and they have

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<v Speaker 1>a number of other cardiovascular problems, but that's besides the point.

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<v Speaker 1>But that's why they were created because when you don't

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<v Speaker 1>target COX one, you don't affect the prostac landids in

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<v Speaker 1>the stomach and you have less gastric problems. So that's

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<v Speaker 1>why nc's are a big issue here. Some other less

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<v Speaker 1>important causes are going to be alcohol, trauma, acute stress,

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<v Speaker 1>radiation and things like that, but the ones you need

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<v Speaker 1>to know is going to be h pylori and n sets.

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<v Speaker 1>Do not forget those H pyloris You're most common and

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<v Speaker 1>says you're second most common costs.

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<v Speaker 2>So remember those.

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<v Speaker 1>As far as the patient presentation, some patients initially may

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<v Speaker 1>be asymptomatic, but as it progresses, you're going to have

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<v Speaker 1>these non specific symptoms. It's like epigastric discomfort also known

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<v Speaker 1>as dyspepsia. They may have some nausea, loss of appetite,

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<v Speaker 1>nothing really specific that you need to know that's gonna

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<v Speaker 1>stick out in a vignette, but just these non specific

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<v Speaker 1>epigastric symptoms. Diagnosing while your test of choice, although it

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<v Speaker 1>isn't necessarily going to be the first thing you do,

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<v Speaker 1>is going to be an upper endoscopy. This is going

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<v Speaker 1>to be your best test. But initially you're going to

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<v Speaker 1>do some testing for H pylori because these are things

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<v Speaker 1>that are non invasive. You can do a uria breath test,

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<v Speaker 1>a fecal antigen test to test for H pylori to

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<v Speaker 1>see if you need to treat that. I'll go over

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<v Speaker 1>those tests a little bit in pepticals or disease and

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<v Speaker 1>what they involve, but those so initially you probably test

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<v Speaker 1>for h uria breath test fecal antigen test, and then eventually,

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<v Speaker 1>if those tests come back negative, these patients are still

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<v Speaker 1>having symptoms, you may move on to an upper endoscopy,

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<v Speaker 1>which would be your best test. And this is going

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<v Speaker 1>to be patients that are refractory to PPIs, H two

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<v Speaker 1>blockers things like that. So some of the ways you

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<v Speaker 1>can diagnose test for H pylori, upper endoscopy, and treatment, well,

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<v Speaker 1>it all depends on the cause. So if these patients

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<v Speaker 1>have H pylori, your test came back positive, you're your

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<v Speaker 1>breath test or vecal antigen test came back positive. You're

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<v Speaker 1>going to treat H pylori. So how do you treat

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<v Speaker 1>H pyloria, whether it's quadruple therapy. Quadruple therapy is going

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<v Speaker 1>to be a combination of PPIs, bismuth, metronidazol, and tetracycling.

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<v Speaker 1>So H pylori positive treat the H pylori with quadruple therapy.

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<v Speaker 1>You want to discontinue n SAID use if that's what's

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<v Speaker 1>causing it, and you can also use PPIs and H

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<v Speaker 1>two blockers, particularly in patients who require the continued use

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<v Speaker 1>of n SET. So whether it's a cardiovascular patient that

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<v Speaker 1>requires daily aspirin patient with chronic pain that has to

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<v Speaker 1>take their ND sets but they develop gastritis, then you

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<v Speaker 1>can use PPIs and H two blockers as well for

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<v Speaker 1>the treatment. So treatment depends on the cause H pylori.

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<v Speaker 1>Treat the H pylori discontinue n said use if they're

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<v Speaker 1>using it, and PPIs and H two blockers are going

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<v Speaker 1>to be your main.

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<v Speaker 2>Ways to treat qute gastritis.

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<v Speaker 1>As something else that I'm going to go over, it's

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<v Speaker 1>definitely not very high yield, but you need to know

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<v Speaker 1>that it exists because it is on the blueprint. It's

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<v Speaker 1>something called autoimmune metaplastic atrophic gastritis, so again not high yield,

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<v Speaker 1>but be aware that it exists. It's a chronic form

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<v Speaker 1>of gastritis. It's an inherited autoimmune disease, so unlike a

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<v Speaker 1>cute gastritis, this isn't going to be from N sets

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<v Speaker 1>or it's pylori use. It's going to be an autoimmune process.

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<v Speaker 1>So the immune system is actually attacking the parietal cells,

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<v Speaker 1>an intrinsic factor in the body. This can lead to

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<v Speaker 1>B twelve deficiency as well as this gastritis that these

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<v Speaker 1>patients have. These patients are also at a high risk

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<v Speaker 1>of gastric carcinoma.

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<v Speaker 2>And one other important thing.

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<v Speaker 1>That you need to know is that while acute gastritis

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<v Speaker 1>most commonly affects the antrum of the stomach, chronic or

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<v Speaker 1>autoimmune gastritis spares the antrum and most commonly affects the

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<v Speaker 1>fundus or the body. So for real life maybe not

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<v Speaker 1>so important, but for a vin yet they may mention that.

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<v Speaker 1>So remember a QT gastritis affects the antrum, chronic autoimmune

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<v Speaker 1>is going to most commonly affect the fundus in the

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<v Speaker 1>body and spares the andantrum. That's really all you need

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<v Speaker 1>to know for that. Don't go crazy again, not very

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<v Speaker 1>high yield.

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<v Speaker 2>Now moving on.

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<v Speaker 1>To something that is high yield is peptic ulcer disease.

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<v Speaker 1>So there's a lot of stuff you need to know

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<v Speaker 1>on this. Let's go over that. There's going to be

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<v Speaker 1>some overlap two with gastritis as well. So peptic ulcer

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<v Speaker 1>disease encompasses both duodenal ulcers and gastric ulcers. So some

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<v Speaker 1>things that two have in common, some things that help

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<v Speaker 1>differentiate them. So we'll go over the different things. So

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<v Speaker 1>let's start with duoden ulcers so duoden ulcers are going

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<v Speaker 1>to be an area of erosion obviously in the duodenum.

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<v Speaker 1>It's going to be your most common type, so much

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<v Speaker 1>more common, about four times more common than gastric ulcers,

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<v Speaker 1>and usually it's benign. Gastric Ulcers are going to be

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<v Speaker 1>an area of erosion in the stomach, and these are

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<v Speaker 1>less prevalent than duodenal ulcers and more commonly associated with

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<v Speaker 1>gastric edinal carcinoma. So remember that duodenal ulcers usually benign.

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<v Speaker 1>Gastric ulcers are more commonly associated with gastric adino carcinoma,

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<v Speaker 1>and duoden ulcers are your more common type as far

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<v Speaker 1>as eteologies, a lot of overlap here with gastritis. Again

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<v Speaker 1>h pylori most common cause overall, nothing new that you

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<v Speaker 1>need to know there, Second most common cause, N SAIDs

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<v Speaker 1>an aspirin really easy. You already know this for gastritis,

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<v Speaker 1>So again hpylori most common. N says an aspirin second

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<v Speaker 1>most common. And then another odd bowl that you need

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<v Speaker 1>to know of that's not very common about you know,

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<v Speaker 1>like less than one percent of patients. It's something called

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<v Speaker 1>Zollinger Ellison syndrome and This is a disease that produces

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<v Speaker 1>high levels of gastrin from a neuroendocrine tumor, and gastrin

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<v Speaker 1>leads to high levels of acid in the stomach, which

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<v Speaker 1>can lead to ulcers and gastritis as well as another

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<v Speaker 1>a few other things. So again not a very common cause,

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<v Speaker 1>but something that you do need to know because it

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<v Speaker 1>may come up in the boards, and just a small

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<v Speaker 1>factor that you need to know as well. So hpylori

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<v Speaker 1>is your most common cause overall, but it's going to

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<v Speaker 1>be more associated with duodeno ulcers, where n sets an asper,

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<v Speaker 1>your second most common cause overall is going to be

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<v Speaker 1>more commonly associated with gaster cultures, So just know that,

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<v Speaker 1>but again same overlap with gastritis. Hpylori most common, and

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<v Speaker 1>sayd as an aspirin second most common, and then just

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<v Speaker 1>know about zolinger ellison just as that oddball that may

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<v Speaker 1>come up, as well as some of the other factors

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<v Speaker 1>you know that can lead to pepic ulcers as well.

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<v Speaker 1>Increased alcohol use, smoking also more common and elderly. Those

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<v Speaker 1>are the less less important things that you need to know.

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<v Speaker 1>But of course hpilor and SAIDs know those. Don't forget

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<v Speaker 1>that as far as the history and exam, these patients

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<v Speaker 1>are going to have some again non specific epigastric pain, burning, nausea,

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<v Speaker 1>they may have early satiety.

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<v Speaker 2>Those things aren't that important.

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<v Speaker 1>It's not going to help you differentiate on of it and yet,

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<v Speaker 1>But what you do need to know with this on

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<v Speaker 1>the history and exam is the different presentation. Do oddinal

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<v Speaker 1>ulcers are going to get better with food? Gastric ulcers

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<v Speaker 1>are going to get worse with food. So why does

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<v Speaker 1>that happen? Well, gastric cultures. When you eat, acids obviously

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<v Speaker 1>released to help break down the food, and so the

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<v Speaker 1>ulcers in the stomach you have pain right away. So

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<v Speaker 1>as soon as you eat, immediately these patients start having pain,

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<v Speaker 1>whereas duadinal ulcers obviously a little bit further down the

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<v Speaker 1>GI tract. As you're eating, the food's kind of shut down,

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<v Speaker 1>it's clamped off, it's churning up in there trying to

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<v Speaker 1>break down the food. So all the acids in the stomach,

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<v Speaker 1>but it's not until about two to five hours later

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<v Speaker 1>that the food starts to be released from the stomach

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<v Speaker 1>enters the duodom. Now these patients start to have pain.

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<v Speaker 1>So while these patients are eating and they have a

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<v Speaker 1>duodin ulcer. They have some relief for about two to

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<v Speaker 1>five hours while the acids still sitting in the stomach.

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<v Speaker 2>Once it starts to come out, then they have pain.

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<v Speaker 1>So duodenal ulcers they're gonna have, They're gonna have relief

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<v Speaker 1>with food. They're gonna see their symptoms improved. Duadinals are

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<v Speaker 1>going to be better with food. Gastric is gonna be

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<v Speaker 1>worse with food. The way I remember that duodenal ulcers.

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<v Speaker 1>Du I remember, dude, give me food?

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<v Speaker 2>Do you do?

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<v Speaker 1>Just like in dude and duodenal? Dude give me food?

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<v Speaker 1>So better with food, duodonal ulcers and gastric.

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<v Speaker 2>Is worse with food.

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<v Speaker 1>And that's why patients with gastric ulcers that the pain

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<v Speaker 1>gets worse with eating. A lot of times you'll see

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<v Speaker 1>weight loss in these individuals compared to duaden ulcers. You

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<v Speaker 1>may see weight gain because their symptoms get better with food,

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<v Speaker 1>so they tend to eat more, So it makes sense.

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<v Speaker 2>One other thing to be.

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<v Speaker 1>Mindful of is that peptic ulcers can bleed and they

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<v Speaker 1>can also perforate, So you need to know that peptic

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<v Speaker 1>ulcers are actually peptic ulcer disease is the most common

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<v Speaker 1>cause of an upper GI bleed. Peptic Ulcer disease most

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<v Speaker 1>common cause of an upper GI bleed. And in the

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<v Speaker 1>case that they do perforate, these patients are going to

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<v Speaker 1>go from this kind of vague epigastric pain pepsia blah

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<v Speaker 1>blah blah, to this sudden onset of this sharp, acute

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<v Speaker 1>abdominal pain. They may have signs of peritonitis like rebound

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<v Speaker 1>tenderness guarding. So know that these peptic ulcers can perforate,

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<v Speaker 1>they can bleed, and the presentation is going to be

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<v Speaker 1>much different. It's obviously a much more serious situation as

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<v Speaker 1>far as diagnosing. Ultimately, your most sensitive and specific test

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<v Speaker 1>is going to be in an endoscopy, But there's a

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<v Speaker 1>few things you want to do before you get to

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<v Speaker 1>an endoscopy. But remember, if an endoscopy is on the

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<v Speaker 1>answer listen it says what is your best test endoscopy,

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<v Speaker 1>it's always going to be the endoscopy. But in real life,

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<v Speaker 1>there's a few things that you're going to do first

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<v Speaker 1>and a few other tests. So if it says what's

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<v Speaker 1>your initial test, you may go with some other things.

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<v Speaker 1>So let's go over that Initially you're probably going to

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<v Speaker 1>test for H. Pylori, So you can do that a

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<v Speaker 1>couple of different ways. You can do a urrea breath

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<v Speaker 1>test or an H. Pylori stool antigen H pylori testing.

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<v Speaker 1>When you do a uria breath test, what you need

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<v Speaker 1>to know about this is is that H. Pylori produces

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<v Speaker 1>an enzyme called urease, which breaks down urrea into ammonia

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<v Speaker 1>and carbon dioxide. So the way this test works is

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<v Speaker 1>that during the test, the patient is given a pill

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<v Speaker 1>containing urea and then they blow into this bag. They

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<v Speaker 1>blow into the bag, they close off the bag, it's

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<v Speaker 1>sent to a lab, and then they test for the

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<v Speaker 1>amount of exhaled carbon dioxide. And remember again they were

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<v Speaker 1>given urea, and as I said before, H pylori turns

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<v Speaker 1>urea into carbon dioxide and ammonia. So if there's an

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<v Speaker 1>increase in all this carbon dioxide that's in this bag,

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<v Speaker 1>then obviously this is gonna be a positive test for H.

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<v Speaker 2>Pylori.

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<v Speaker 1>So that's how a urrea breath test works. H Pylori

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<v Speaker 1>stool intogen is straightforward. It's literally just checking for a

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<v Speaker 1>stool antigen of H.

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<v Speaker 2>Pylori.

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<v Speaker 1>So that's another test that you can do as well.

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<v Speaker 1>And then ultimately, like I said before, the gold standard

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<v Speaker 1>test is going to be your endoscopy. That's going to

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<v Speaker 1>be to diagnose. You can visualize the ulcer and you

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00:12:21.799 --> 00:12:24.919
<v Speaker 1>can take biopsies if needed, and then treatment depends on

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00:12:24.960 --> 00:12:28.000
<v Speaker 1>the cause. So let's start with H pylori. If this

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<v Speaker 1>patient is H pylori positive, again, just like in guesstritis,

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<v Speaker 1>you're going to do quadruple therapy. The way I remember

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<v Speaker 1>quadruple therapy for an hpylori positive patient is I remember

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00:12:38.480 --> 00:12:41.600
<v Speaker 1>these patients have belly pain. They want you to treat

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00:12:41.600 --> 00:12:43.399
<v Speaker 1>their belly pain so they can get better. So they

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<v Speaker 1>say to you, treat my belly, please, treat my belly please.

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<v Speaker 1>TMBP that stands for tetracycling, metronideisol, bismyth subseliciy, and PPIs

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<v Speaker 1>treat my belly please. Tetracycling, metronide, is al, bismuth, subselicily,

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<v Speaker 1>and P. Those are for your H. Pylori positive patients. Now,

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<v Speaker 1>if these patients are hpylori negative, how do you treat

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<v Speaker 1>their peptic ulcer disease? Well, first, treat the underlying cause.

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<v Speaker 1>If they're taking nsids, they're smokers, they drink a bunch

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<v Speaker 1>of alcohol. You're going to discontinue all those things obviously,

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<v Speaker 1>and then you're going to give them PPIs as well.

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<v Speaker 1>You can also use H two blockers, but realistically, anytime

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<v Speaker 1>you have an option of a PPI or an H

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<v Speaker 1>two blocker, unless there's some contraindication of PPIs, always use PPIs.

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<v Speaker 1>Why is that PPIs are much more effective, and that's because,

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<v Speaker 1>I mean, just really quickly break down the way these

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00:13:37.039 --> 00:13:38.639
<v Speaker 1>work and just to give you a little bit about

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<v Speaker 1>the may of the mets. So you have a parietal

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<v Speaker 1>cell in the stomach. The parietal cell has a proton pump.

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<v Speaker 1>That's what shoots out all the hydrochloric acid into the stomach.

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<v Speaker 1>That's where all of your acid in the stomach comes from.

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<v Speaker 1>So how is your prietal cell activated. Well, acetylcholine, histamine,

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<v Speaker 1>and gastrin all activate the prietal cell to pump out

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<v Speaker 1>this acid. An H CH two blocker obviously blocks H

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00:14:02.440 --> 00:14:05.639
<v Speaker 1>two and that's histamine, So that's a histamine blocker, So

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00:14:05.720 --> 00:14:09.360
<v Speaker 1>it blocks just histamine, but you still have acetocholine and

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00:14:09.399 --> 00:14:12.480
<v Speaker 1>gastrine that can activate the parietal cell. So while it

290
00:14:12.639 --> 00:14:15.879
<v Speaker 1>helps because you stop the histamine from activating the paryal cell.

291
00:14:16.039 --> 00:14:18.840
<v Speaker 1>Stylcholine and gastrine are still working there to pump out acid,

292
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<v Speaker 1>so there's still some acid production, Whereas a proton pump

293
00:14:22.159 --> 00:14:26.200
<v Speaker 1>inhibitor actually completely shuts off the proton pump, so it

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00:14:26.200 --> 00:14:28.639
<v Speaker 1>doesn't matter how much is stylcholine, how much histamine, how

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00:14:28.679 --> 00:14:32.120
<v Speaker 1>much gastrine is activating that parietal cell. The pump is

296
00:14:32.159 --> 00:14:35.159
<v Speaker 1>shut off, so no acids coming out. So PPIs are

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00:14:35.240 --> 00:14:37.440
<v Speaker 1>much more effective. So remember, if you have an option

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00:14:37.519 --> 00:14:40.159
<v Speaker 1>of a PPI or hto blocker, use the PPI. So

299
00:14:40.200 --> 00:14:44.080
<v Speaker 1>again H pylor negative, treat the underlying cause, give them PPIs.

300
00:14:44.360 --> 00:14:47.279
<v Speaker 1>That's the treatment. If they're H pylori positive, treat the

301
00:14:47.399 --> 00:14:50.639
<v Speaker 1>H pylori very easy treatment. And then there's one other

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00:14:50.679 --> 00:14:54.480
<v Speaker 1>treatment option that you should probably know. For refractory patients.

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00:14:54.519 --> 00:14:58.679
<v Speaker 1>The PPIs aren't working, you discontinued all the ensis, et cetera,

304
00:14:58.960 --> 00:15:01.320
<v Speaker 1>and they're still having SIN, you can do something called

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00:15:01.320 --> 00:15:04.519
<v Speaker 1>the parietal cell veagotomy, which is where they sever the

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00:15:04.600 --> 00:15:09.000
<v Speaker 1>vagual nerve, which essentially shuts down the portion of the

307
00:15:09.039 --> 00:15:12.440
<v Speaker 1>stomach where the parietal cells are located. And this obviously

308
00:15:12.519 --> 00:15:15.759
<v Speaker 1>leads to decreased acid by about seventy five percent, So

309
00:15:15.799 --> 00:15:18.639
<v Speaker 1>pretty effective procedure, but it's invasive. Obviously, there's a lot

310
00:15:18.679 --> 00:15:20.320
<v Speaker 1>of things you want to try before you get to

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00:15:20.360 --> 00:15:22.240
<v Speaker 1>a parietal cell vegotamin. This is just going to be

312
00:15:22.240 --> 00:15:25.080
<v Speaker 1>for your refractory patients. So those are the treatments. Let's

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00:15:25.120 --> 00:15:26.879
<v Speaker 1>move on to the home stretch here. The last thing

314
00:15:26.879 --> 00:15:28.039
<v Speaker 1>we're going to go over, and that's going to be

315
00:15:28.039 --> 00:15:30.720
<v Speaker 1>pyloric stenosis. So this is going to be a condition

316
00:15:30.960 --> 00:15:33.879
<v Speaker 1>commonly in newborns. About three to six weeks is going

317
00:15:33.919 --> 00:15:36.279
<v Speaker 1>to be your most common age range, and it's a

318
00:15:36.320 --> 00:15:42.000
<v Speaker 1>thickening hypertrophy, a thickening or hypertrophy of the pyloris, which

319
00:15:42.039 --> 00:15:45.080
<v Speaker 1>is the sphincter, the muscular valve between the stomach and

320
00:15:45.120 --> 00:15:49.399
<v Speaker 1>the duodenum, so it prevents gastric emptying. Risk factors are

321
00:15:49.440 --> 00:15:52.399
<v Speaker 1>going to be males four times more common in male,

322
00:15:52.480 --> 00:15:55.200
<v Speaker 1>so definitely know that males are going to be much

323
00:15:55.200 --> 00:15:58.279
<v Speaker 1>more common. Look at your vignette. If it's a female,

324
00:15:58.720 --> 00:16:00.519
<v Speaker 1>you know for a vignette probably and that's so common

325
00:16:00.519 --> 00:16:03.000
<v Speaker 1>that it's going to be pylar scinosis. Three to six

326
00:16:03.039 --> 00:16:05.360
<v Speaker 1>weeks is going to be your most common age of presentation.

327
00:16:05.720 --> 00:16:08.440
<v Speaker 1>Sometimes they'll say three to twelve, but generally three to

328
00:16:08.480 --> 00:16:11.519
<v Speaker 1>six is the most common. And then first born patients

329
00:16:11.519 --> 00:16:13.240
<v Speaker 1>are also going to be at a higher risk. And

330
00:16:13.279 --> 00:16:15.919
<v Speaker 1>then the last thing too, not as you know, not

331
00:16:15.960 --> 00:16:17.639
<v Speaker 1>as big of a risk as the other ones, but

332
00:16:17.799 --> 00:16:22.279
<v Speaker 1>macrolide antibiotics, in particular erythromycin within the first two weeks

333
00:16:22.720 --> 00:16:26.200
<v Speaker 1>of birth can also lead to pyloric stenosis. And this

334
00:16:26.360 --> 00:16:29.600
<v Speaker 1>is the way it's explained, is most likely due to

335
00:16:29.639 --> 00:16:33.840
<v Speaker 1>the increased gastric motility with macrolight antibiotics. Erythromycin, even a

336
00:16:33.919 --> 00:16:37.240
<v Speaker 1>zythromycin can cause this. So the increased gastric motility in

337
00:16:37.279 --> 00:16:40.279
<v Speaker 1>these drugs can lead to hypertrophy from the pyloris basically

338
00:16:40.320 --> 00:16:43.200
<v Speaker 1>just being overworked. And it's the same reason that we

339
00:16:43.320 --> 00:16:47.360
<v Speaker 1>use erythromycin and gastroparesis because it increases the gimotility. So

340
00:16:47.399 --> 00:16:49.480
<v Speaker 1>if you have a patient under two weeks they give

341
00:16:49.519 --> 00:16:52.200
<v Speaker 1>them a erythromycin, this may lead to pyloric stenosis. So

342
00:16:52.279 --> 00:16:55.639
<v Speaker 1>risks again males first born three to six weeks of

343
00:16:55.679 --> 00:16:59.240
<v Speaker 1>life and macrolide antibiotics in particular erythromycin. All right, So

344
00:16:59.519 --> 00:17:02.559
<v Speaker 1>as far as the history and the exam. They may

345
00:17:02.600 --> 00:17:06.599
<v Speaker 1>have some non specific symptoms weight loss, dehydration doesn't matter.

346
00:17:06.680 --> 00:17:08.319
<v Speaker 1>You don't care about that stuff because it's not going

347
00:17:08.359 --> 00:17:11.079
<v Speaker 1>to help you differentiate it in Yet, what you need

348
00:17:11.119 --> 00:17:14.079
<v Speaker 1>to know for pylor ex stenosis, there's two really big

349
00:17:14.119 --> 00:17:19.359
<v Speaker 1>things you cannot forget. So pilar stenosis non bilious projectile

350
00:17:19.440 --> 00:17:22.160
<v Speaker 1>vomiting after feeding. That is going to be your vignette

351
00:17:22.240 --> 00:17:24.400
<v Speaker 1>right there. You can just go ahead and circle pilar stenosis.

352
00:17:24.480 --> 00:17:26.440
<v Speaker 1>That's gonna be your answer. So you see non bilious

353
00:17:26.440 --> 00:17:29.839
<v Speaker 1>projectile vomiting after feeding pilar stenosis. So why is it

354
00:17:29.960 --> 00:17:33.599
<v Speaker 1>non bilious? Well, remember this is an obstruction at the stomach.

355
00:17:33.640 --> 00:17:36.519
<v Speaker 1>It's at the pylorus, so we're not into the area

356
00:17:36.519 --> 00:17:38.759
<v Speaker 1>where the bile is coming from the common bioduct. It's

357
00:17:38.799 --> 00:17:41.880
<v Speaker 1>not evolves. It's an unomal rotation of the small bowel,

358
00:17:41.920 --> 00:17:43.559
<v Speaker 1>so we're not in the area where the bile is

359
00:17:43.599 --> 00:17:46.839
<v Speaker 1>being excreted. So it's gonna be non bilious. It's in

360
00:17:46.880 --> 00:17:50.200
<v Speaker 1>the stomach, So non bilious projectile vomiting after feeding that

361
00:17:50.359 --> 00:17:53.359
<v Speaker 1>is going to be pathonomoonic, almost as pathonomonic as The

362
00:17:53.400 --> 00:17:55.119
<v Speaker 1>second thing you need to know for the exam and

363
00:17:55.160 --> 00:17:58.000
<v Speaker 1>that's going to be an olive shaped mass. So on

364
00:17:58.079 --> 00:18:01.720
<v Speaker 1>physical exam, we talked about the the pyloris being hypertropheed.

365
00:18:01.759 --> 00:18:04.960
<v Speaker 1>It's enlarged, and on physical exam, normally you're not gonna

366
00:18:04.960 --> 00:18:07.119
<v Speaker 1>be able to feel the pylorus. But these patients, because

367
00:18:07.119 --> 00:18:10.599
<v Speaker 1>it's hypertrop feed, you're actually going to feel this olive

368
00:18:10.640 --> 00:18:14.440
<v Speaker 1>shaped mass in the epigastric area and it's going to

369
00:18:14.480 --> 00:18:16.759
<v Speaker 1>feel like a small round mass and it's described as

370
00:18:16.799 --> 00:18:20.559
<v Speaker 1>an olive shaped mass. If you see this on a vignette,

371
00:18:20.680 --> 00:18:22.559
<v Speaker 1>you see this or you feel this in real life,

372
00:18:22.599 --> 00:18:25.640
<v Speaker 1>this is really pathdomonic for the disease. And actually, years ago,

373
00:18:25.720 --> 00:18:29.680
<v Speaker 1>before ultrasound was around, this would be the only way

374
00:18:29.680 --> 00:18:31.720
<v Speaker 1>you would diagnose it. If you felt this olive shaped mass,

375
00:18:31.720 --> 00:18:34.000
<v Speaker 1>they would go right to surgery, you know, after you

376
00:18:34.119 --> 00:18:36.720
<v Speaker 1>treated them with fluids and things like that. So physical

377
00:18:36.759 --> 00:18:41.119
<v Speaker 1>exam no non bilious projectile vomiting and no olive shaped mass.

378
00:18:41.119 --> 00:18:42.440
<v Speaker 1>So those are the two things you need to know

379
00:18:42.559 --> 00:18:45.319
<v Speaker 1>as far as diagnosing. Ultrasound is going to be your

380
00:18:45.359 --> 00:18:48.240
<v Speaker 1>test of choice. It's ninety seven to ninety nine percent

381
00:18:48.400 --> 00:18:50.079
<v Speaker 1>sensitive no radiation.

382
00:18:50.160 --> 00:18:50.920
<v Speaker 2>These are newborns.

383
00:18:50.920 --> 00:18:52.440
<v Speaker 1>You really don't want to radiate them if you don't

384
00:18:52.480 --> 00:18:54.400
<v Speaker 1>have to. And then on the ultrasound, you're going to

385
00:18:54.440 --> 00:18:58.119
<v Speaker 1>see some pyloric muscle thickness over four millimeters and the

386
00:18:58.160 --> 00:19:00.960
<v Speaker 1>pyloric canal length will be over seven eighteen millimeters. Don't

387
00:19:00.960 --> 00:19:03.079
<v Speaker 1>worry about those numbers, but I just want to throw

388
00:19:03.119 --> 00:19:05.200
<v Speaker 1>that out there so you know that's how you actually

389
00:19:05.400 --> 00:19:06.559
<v Speaker 1>have a positive ultrasound.

390
00:19:06.559 --> 00:19:08.200
<v Speaker 2>But ultra sound is gonna be your test of choice.

391
00:19:08.240 --> 00:19:09.839
<v Speaker 1>The only reason I'm even going to mention an upper

392
00:19:09.839 --> 00:19:11.559
<v Speaker 1>GI series not so much that you're going to use

393
00:19:11.559 --> 00:19:12.920
<v Speaker 1>it in real life. It's really only going to be

394
00:19:12.920 --> 00:19:17.079
<v Speaker 1>if ultrasounds inconclusive, the physical exam is inconclusive. But you

395
00:19:17.160 --> 00:19:18.960
<v Speaker 1>need to know for the exam because on an upper

396
00:19:18.960 --> 00:19:21.000
<v Speaker 1>GI series, there's a couple of key terms.

397
00:19:21.200 --> 00:19:22.759
<v Speaker 2>There's one called a string sign.

398
00:19:22.799 --> 00:19:26.200
<v Speaker 1>It's not specific only to pyloxynosis, but if you do

399
00:19:26.279 --> 00:19:28.559
<v Speaker 1>see it in this vignette, this is going to be

400
00:19:28.599 --> 00:19:32.000
<v Speaker 1>a narrowed area of barium flow. It's literally going to

401
00:19:32.079 --> 00:19:35.160
<v Speaker 1>look like a string of barium because that hypertro feed

402
00:19:35.160 --> 00:19:37.960
<v Speaker 1>area only allowing a small amount of barium through. So

403
00:19:37.960 --> 00:19:40.319
<v Speaker 1>that's a string sign and upper GI. And there's another

404
00:19:40.400 --> 00:19:43.559
<v Speaker 1>one called a railroad track sign, and this is due

405
00:19:43.640 --> 00:19:49.240
<v Speaker 1>to the pyloric mucosa compressing and pushing causing this double

406
00:19:49.319 --> 00:19:52.359
<v Speaker 1>canal where you're going to see two small tracks of

407
00:19:52.400 --> 00:19:54.599
<v Speaker 1>barium flowing through. It kind of looks like a railroad

408
00:19:54.759 --> 00:19:57.000
<v Speaker 1>and that's a railroad sign on upper GI. So again

409
00:19:57.039 --> 00:19:59.160
<v Speaker 1>in real life, probably not going to do an UPPERGI,

410
00:19:59.279 --> 00:20:01.240
<v Speaker 1>but you do need to know for the exams because

411
00:20:01.279 --> 00:20:02.960
<v Speaker 1>they like to throw out these key terms of string

412
00:20:03.039 --> 00:20:05.920
<v Speaker 1>sign and railroad track sign on what you'll see on UPPERGI.

413
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<v Speaker 1>And then as far as labs, they're vomiting up all

414
00:20:08.240 --> 00:20:13.359
<v Speaker 1>the stomach acids, so you may have this hypochloromic metabolic acidosis.

415
00:20:13.519 --> 00:20:17.079
<v Speaker 1>They may also have hypokalmia, and this is just because

416
00:20:17.279 --> 00:20:20.720
<v Speaker 1>the kidney's compensating and flushing out all of the renal

417
00:20:20.759 --> 00:20:26.200
<v Speaker 1>potassium excretion. So hypochloromic metabolic acidosis may be seen. And

418
00:20:26.240 --> 00:20:29.400
<v Speaker 1>then they also may have hypokalemia on labs. But your

419
00:20:29.480 --> 00:20:31.519
<v Speaker 1>key for diagnosis is going to be your ultrasound. But

420
00:20:31.559 --> 00:20:34.000
<v Speaker 1>know these things as well. So as far as treatment,

421
00:20:34.599 --> 00:20:38.039
<v Speaker 1>initially these patients can be kind of sick. They're volume depleted,

422
00:20:38.359 --> 00:20:40.519
<v Speaker 1>so before you get to any intervention, you need to

423
00:20:40.559 --> 00:20:44.200
<v Speaker 1>start with some fluids. You want to do electrolyte replacement.

424
00:20:44.240 --> 00:20:46.680
<v Speaker 1>Remember again I said they may be HYPOKLEMICX you want

425
00:20:46.680 --> 00:20:49.759
<v Speaker 1>to replace the potassium, may give them some dextros IV

426
00:20:49.839 --> 00:20:52.720
<v Speaker 1>fluids and things like that. Once they're euvulymic, then you

427
00:20:52.759 --> 00:20:54.799
<v Speaker 1>get to the actual procedure that needs to be done

428
00:20:54.799 --> 00:20:57.599
<v Speaker 1>in these patients. And this is called the pyloral miotomy

429
00:20:57.839 --> 00:20:59.440
<v Speaker 1>is the name of the procedure that you want to

430
00:20:59.480 --> 00:21:03.640
<v Speaker 1>do once they're stable their euvolemic and this is normally

431
00:21:03.640 --> 00:21:08.400
<v Speaker 1>done laparoscopically. The surgeon makes this longitudinal incision into the

432
00:21:08.400 --> 00:21:12.759
<v Speaker 1>pylorus and once they make this longitudinal incision, that hypertrophied

433
00:21:12.880 --> 00:21:16.319
<v Speaker 1>muscle kind of pops out through this incision that they made.

434
00:21:16.480 --> 00:21:19.920
<v Speaker 1>And once it pops up through this area of the incision,

435
00:21:20.480 --> 00:21:23.960
<v Speaker 1>now beneath the area of the incision, there's this canal

436
00:21:24.000 --> 00:21:26.319
<v Speaker 1>that opened up this new space because all the muscle

437
00:21:26.400 --> 00:21:29.000
<v Speaker 1>kind of tunneled up through this incision, and they actually

438
00:21:29.160 --> 00:21:32.480
<v Speaker 1>have this area where the stomach contents can flow through

439
00:21:32.480 --> 00:21:36.839
<v Speaker 1>this area, so that again it's called a pyloromiotomy. Pyloromotomy

440
00:21:37.000 --> 00:21:39.440
<v Speaker 1>is going to be the treatment of choice once these

441
00:21:39.440 --> 00:21:43.000
<v Speaker 1>patients are stable and euvolemic, so that's what you need

442
00:21:43.039 --> 00:21:45.640
<v Speaker 1>to know. Those are the main things. I feel like

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<v Speaker 1>I kind of touched on all the high yield stuff.

444
00:21:48.400 --> 00:21:51.559
<v Speaker 1>I hope that was helpful. And as always, good luck

445
00:21:51.640 --> 00:21:54.480
<v Speaker 1>on your pants, your panry, your ear, and good luck

446
00:21:54.519 --> 00:22:00.039
<v Speaker 1>in PA school and
